80 / 162
Support:
These studies were completed as part of an interdisci-
plinary research team funded by The Moody Project for Translational
Traumatic Brain Injury
Keyword: Chronic
C2-10
PATHWAY ANALYSIS OF NEUROPROTECTIVE DRUG
TREATMENT AFTER ACUTE TRAUMATIC BRAIN INJURY
Debbie Boone
, Harris Weisz, Douglas DeWitt, Donald Prough, Helen
Hellmich
University of Texas Medical Branch, Anesthesiology, Galveston, USA
Background:
The current lack of therapeutic agents for treatment of
TBI patients highlights a compelling need to explore and test new drug
candidates. We identified two novel compounds that reduce neuronal
injury and inflammation; JM6, an experimental neuroprotective drug
used in animal models of Alzheimer’s and Huntington’s disease, and
clovanemagnolol, a natural compound with neuro-regenerative proper-
ties. Here, we test our hypothesis that the neuroprotective effects of these
two compounds are mediated by a common set of genes/ pathways.
Methods:
Isoflurane-anesthetized, Male-Sprague Dawley rats (300
to 350 g) received a severe fluid percussion injury. One hour post
injury, rats were dosed with JM6 (400 mg/kg oral gavage) or Clova-
nemagnolol (2 mg/kg IP injection). Reduction of neuronal injury and
microglial activation was assessed by Fluoro-Jade C (FJC) staining
and immunohistochemistry, with an antibody to CD11b. We used
Laser Capture Microdissection to collect neurons from the hippo-
campal CA1-CA3 regions. Total RNA was sent to GenUs Biosystems
for genome-wide microarray analysis (Agilent Rat GE 8x60K arrays).
Gene expression data were analyzed with GeneSpring GX and filtered
gene lists (
>
1.5 Fold, p
<
0.05, Sham vs. TBI, TBI vs. JM6, TBI vs.
CM) were uploaded into Ingenuity Pathway Analysis. We validated
individual gene changes using Real-Time PCR.
Results:
JM6 and Clovanemagnolol significantly (p
<
0.05) reduced
the number of FJC- positive hippocampal neurons and reduced mi-
croglial activation in the rat brain. Our analysis showed that JM6 and
Clovanemagnolol similarly altered expression of genes that were
significantly dysregulated after TBI. The affected pathways (PPAR
signaling, axonal guidance signaling and Wnt signaling) are associ-
ated with cell survival, synaptic plasticity and development.
Conclusion:
JM6 and Clovanemagnolol appear to reduce post-
traumatic neurodegeneration by restoring TBI- dysregulated gene
expression to sham control levels. Novel drug candidates with similar
mechanisms of action could be neuroprotective.
Support: These studies were completed as part of an interdisci-
plinary research team funded by The Moody Project for Translational
Traumatic Brain Injury.
Keywords: Drug
C3 Poster Session V - Group C: Neurocritical Care
C3-01
THE INFLUENCE OF INSURANCE STATUS ON SPINE
TRAUMA PATIENT TRANSFERS AT A LEVEL I TRAUMA
CENTER WITH A LARGE CATCHMENT AREA
Maya Babu
, William Krauss, John Atkinson, Donald Jenkins,
Michelle Clarke
Mayo Clinic, Neurologic Surgery, Rochester, USA
Introduction:
The influence of insurance status upon patient transfers
(between Level II/III centers and Level I centers) during certain days
of the week for mild head injury has been described in the literature.
In this study, we investigate whether there is a relationship between
insurance status and the day of transfer for spine trauma patients at
one Level I trauma center.
Methods:
We reviewed all 734 records of patient transfers to one
Level One Trauma Center (Saint Mary’s Hospital, Rochester MN)
from 2007–2014 for spine trauma. Age, Sex, Race, Marital Status,
Insurance Status (Private Insurance, Medicaid, Medicare, Automobile
Insurance, Self-Pay), Transferring Hospital Location, Length of Stay,
Intervention Performed (egs. fusion, percutaneous vertebroplasty),
Admitting Service, Co-Morbidities and Cervical, Thoracic, and
Lumbar Spine Trauma (by ICD-9 Diagnostic Codes) were included.
STATA software was used for multivariate regression analyses.
Results:
We found that transfers on Saturdays for spine trauma re-
quiring intervention is twice as likely if a patient has Medicare than
other forms of insurance (OR
=
2.0, CI
=
[1.062–3.813]). Transfers on
Mondays for spine trauma requiring intervention is likely not to occur if
the patient has Medicare (OR
=
.394, CI
=
[.199–.783]) or is privately
insured (OR
=
.408, CI
=
[.181–.919]). Transfers on the remaining days
of the week did not show a significant relationship with insurance status.
Conclusion:
In this study of a single Level I Trauma Center over
seven years, we found a relationship between insurance status and pa-
tient transfer, such that patients on Medicare tend to be transferred out
at higher rates on Saturday. The temporal relationship is curious, and
may be due to staffing issues at Level II or III centers, or due to gaps in
coverage by specialists. If transfers to Level I centers for weekend care
are made out of convenience and not necessity, this raises ethical
concerns as to where and when optimal patient care should occur.
Keywords: Spine Trauma, Spine Injuries, EMTALA, Patient
Transfer, Level I Center
C3-02
TREATMENT OF TRAUMATIC NON-CONVEXITY SUB-
DURAL HEMORRHAGE IS SIMILAR TO TREATMENT OF
TRAUMATIC SUBARACHNOID HEMORRHAGE
Benedicto Baronia
1
, Yazan Al-Hasan
2
1
Texas Tech University Health Sciences Center, Dept of Surgery -
Neurosurgery, Lubbock, USA
2
Texas Tech University Health Sciences Center, School of Medicine,
Lubbock, Texas
We consider tentorial and interhemispheric subdural hematomas to be
non-convexity subdural hematoma (ncSDH) and should proceed with a
similar benign course as traumatic subarachnoid hemorrhage (tSAH).
Retrospective review of 180 pts who presented acutely to the Emergency
Department with intracranial bleeds secondary to trauma found that pa-
tients with ncSDH rarely required catheter placement or craniotomy (2
interhemispheric and 0 tentorial). Furthermore, recovery of ncSDH was
similar to tSAH. Indications for surgical intervention are generally de-
rived from convexity SDH (cSDH). These criteria include: hematoma
volume of
‡
30 cc, midline shift of
‡
5mm and presence of neurological
signs. However, in elderly populations not exhibiting neurological signs
regardless of hematoma volume and midline shift, operative procedures
could lead to unnecessary risks and interventions. We hypothesize that
the pressure vector generated by ncSDH does not lead to significant
pathophysiologic mechanisms, e.g., brain herniation, mass effect, as
compared to the more common cSDH. This protection could be con-
ferred by the direction of the pressure exerted against the thick mem-
branes of the falx cerebri and tentorium cerebelli in ncSDH. Furthermore,
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